The ocular lens normally exists in an environment of high oxidative stress which is manifested in the occurrence of marked oxidative modification to lens proteins during aging and particularly during cataract development. We are engaged in characterizing such protein changes and elucidating the mechanisms which produce them. Model systems are used to study changes produced in organ cultured lenses or in crystallin solutions. Complex interactions among the various forms of activated oxygen are involved in the damage produced in such model systems and very probably in the lens in vivo as well. The potential of the various activated oxygen species to produce damage depends upon where they are generated, ie, inside the lens or in the external milieu. Understanding the interactions among the oxidant species and lens components is essential if we are to devise therapeutic means to prevent oxidative damage. The study of animal colonies with hereditary cotaract has provided numerous insights into processes of cataractogenesis. We have begun to investigate the nuclear cataracts present congenitally in a colony of guinea pigs. Dr. Q-L. Huang has isolated and described the crystallins from normal guinea pigs so that they can be compared with crystallins from the cataractous animals. The discovery of a new crystallin not present in other species raises exciting possibilities for study of gene expression in the lens. Transport processes are vital to the maintenance of normal lens homeostasis. Dr. V. A. Lucas is studying the membrane protein present in lens which transports glucose across cell membranes. This glucose transporter has been isolated and an antibody raised against it. Characterization of glucose transport in monkey lens membranes has been done using specific binding assays and known inhibitors of the glucose transporter.